Both bisphosphonates and denosumab prevent bone loss; additionally, denosumab has proven anti-fracture benefit in post-menopausal women receiving aromatase inhibitors for hormone receptor-positive breast cancer.
The analysis of the CYP19A1rs749292 polymorphism showed that there were no statistically significant differences in the distribution of genotypes between the study groups with osteoporosis and osteopenia and the control group.
Standard adjuvant therapies for breast cancer such as chemotherapy or aromatase inhibitor and LH-RH agonist hormone therapy are associated with significant survival gains but also induce bone loss by aggravating the estrogen deprivation.
Osteoporosis (OP) risk factor assessment and bone mineral density (BMD) testing are frequently omitted at baseline in aromatase inhibitor (AI) studies, which may lead to misinterpretation of AI associated bone loss.
Adjuvant aromatase inhibitor (AI) therapy, for hormone receptor-positive breast cancer, in postmenopausal women is associated with bone loss, leading to an increased risk of fractures.
Effect of denosumab on bone mineral density in Japanese women with osteopenia treated with aromatase inhibitors for breast cancer: subgroup analyses of a Phase II study.
Adjuvant use of gonadotropin-releasing hormone analogues, which can also be used in metastatic disease, in combination with tamoxifen in premenopausal women, and aromatase inhibitors in postmenopausal women with hormone-sensitive breast cancer, causes rapid bone loss and fragility fractures.
Aromatase inhibitors (AIs) play an important role in the adjuvant treatment of hormone receptor-positive breast cancer, but they are associated with bone loss and increased fracture risk.
Women receiving adjuvant aromatase inhibitors and the subset of premenopausal woman treated with tamoxifen have accelerated bone loss and increased fracture risk.
Although adjuvant aromatase inhibitor (AI) therapy is widely used in postmenopausal women with hormone receptor-positive breast cancer, it is known to be associated with bone loss and increased fracture risk.
It is well known that anti-estrogen therapy (AET), especially aromatase inhibitors (AI), is associated with rapid bone loss and thus increases the risk of osteoporosis.
These agents are also approved at lower doses for the treatment of patients with postmenopausal osteoporosis, a population largely overlapping with those in the early stages of breast cancer, and those with cancer treatment-induced bone loss, which is caused primarily by aromatase inhibitors.
Although, third-generation aromatase inhibitors (AIs) are used as first-line treatment in post-menopausal women, they cause endocrine resistance and bone loss, which limits their success.
Our findings suggest the usefulness of addition of risedronate in order to prevent aromatase inhibitors-related bone loss, not only in case of high-risk of fractures, but also for women at mild-moderate risk.
About half of the 391 patients treated with AIs in the Barcelona-Aromatase induced bone loss in early breast cancer cohort suffered a significant bone loss at lumbar spine (LS) and/or femoral neck (FN) after 2 years on AI-treatment.
Age, breast cancer history, prior chemotherapy, and tamoxifen or aromatase inhibitor (AI) use were not associated with having osteoporosis or osteopenia.
Polymorphisms in the CYP19A1 (aromatase) gene influence disease-free survival and bone loss in patients taking aromatase inhibitors (AIs) for estrogen receptor-positive (ER+) breast cancers.
The objective of this study is to determine the influence of polymorphisms in the CYP19A1 gene on bone loss among patients taking aromatase inhibitors for ER+ breast cancer.
Moreover, with aging, individual differences in aromatase activity and thus in estrogen levels may significantly affect bone loss and fracture risk in both genders.